Accelerated atherosclerosis in Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis: case report

ABSTRACT Accelerated atherosclerosis has been identified as a complication of multiple autoimmune diseases, among which Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis stands out. We describe the case of a 60-year-old patient with a history of hypertension, diabetes mellitus, and chronic kidney disease of unknown etiology, who presented two acute coronary syndromes with only a six-month difference. Rapid progression of coronary involvement was evidenced, along with increased markers of inflammatory response, usual interstitial pneumonia on tomography, and positive anti-myeloperoxidase antibodies (anti-MPO), leading to the diagnosis of microscopic polyangiitis (MPA). In these cases, timely diagnostic suspicion is crucial, as early treatment significantly impacts the course and prognosis of the disease.


Introduction
Vasculitis are a group of disorders characterized by inflammation of the blood vessels, endothelial injury, and tissue damage with clinical manifestations that vary according to the type of vessel affected.One of the rare conditions of vasculitis is involvement of the coronary arteries (1,2) .We present the case of a woman with acute coronary syndrome, in whom vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA) with renal, pulmonary, and coronary involvement secondary to accelerated atherosclerosis was documented.Dual antiplatelet therapy and high-intensity statins were prescribed, which she adhered to adequately during oupatient follow-up.

Case report
A 60-year-old woman with a history of hypertension, type A retrospective extramural search was also conducted, and a report of the renal biopsy performed at the time of diagnosis of kidney disease was found, which concluded in necrotizing glomerulonephritis with extracapillary proliferation in a chronic phase.This led to a diagnosis of microscopic polyangiitis (MPA) with renal, pulmonary (interstitial) involvement and accelerated coronary atherosclerosis.Finally, management included methylprednisolone 500 mg/day for 3 days, followed by prednisolone 30 mg/day with a clearance plan, and rituximab 1 g (day 0-14).It was deemed appropriate to wait until disease activity was controlled before proceeding with revascularization safely.

Discussion
The clinical case illustrates a cardiac manifestation that, although rare, leads to significant morbidity and mortality.While the association between cardiovascular diseases and chronic inflammatory conditions is well described in patients with ANCA-associated vasculitis (AAV) (1) , cardiac involvement poses a diagnostic challenge and requires a high clinical suspicion leading to timely intervention, as was the case in our patient.
Cardiovascular disease in autoimmune diseases can arise from various mechanisms, including accelerated atherosclerosis, valvular disease, systemic, myocardial and/or vascular inflammation, as well as myocardial ischemia secondary to microvascular, macrovascular, or direct coronary artery disease, which can lead to secondary myocardial fibrosis (2) .
Vasculitis causes vascular involvement through the direct leukocytes invasion into the walls of blood vessels, generating disproportionate inflammation that can lead to occlusion, stenosis, aneurysm, and/or rupture, or the development of premature atherogenesis (3) .TNFα-mediated production of proinflammatory cytokines, mainly IL-1 and IL-6, is described, which leads to endothelial injury, blood vessel occlusion, and ischemia, resulting in organ damage.The necrosis of endothelial cells and detachment of the basement membrane not only provide a potential biomarker of disease activity but are also harmful.These structures derived from platelet activation and dead endothelial cell remnants form microparticles that have been associated with the formation of unstable plaques, known to mediate adverse cardiovascular events (1,5) .
Atherosclerosis in AAV has been described in several studies reporting endothelial dysfunction, increased arterial stiffness measured by pulse wave velocity, and increased intima thickness (6) .This phenomenon is characterized by abnormal Figura 1. (A) Initial coronary angiography showing a non-significant lesion in the first diagonal artery (black arrow).(B) Initial coronary angiography with dominant right coronary artery without lesions.(C) Second coronary angiography showing severe 70% stenosis of the proximal circumflex artery (white arrow) and severe lesions at the origin (white arrowhead) and proximal third (black arrowhead) of the obtuse marginal branch.D) Second coronary angiography showing severe 80% stenosis in the distal third of the right coronary artery (black arrowhead).
accumulation of oxidized LDL in the arterial intima, leading to recruitment of monocytes, macrophages, phagocytosis, and activation and release of cytokines.Adaptive immunity plays an important role in pathophysiology as do neutrophil extracellular traps and the inflammasome.Recent evidence suggests that cholesterol crystals can induce activation of the innate immune system through assembly of the NLRP3 protein of the inflammasome (Nod-like receptor family pyrin domain-containing-3) resulting in production of IL-1β and IL-